Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia
Nature Communications, ISSN: 2041-1723, Vol: 5, Issue: 1, Page: 5316
2014
- 222Citations
- 264Captures
- 2Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations222
- Citation Indexes222
- 222
- CrossRef196
- Captures264
- Readers264
- 264
- Mentions2
- Blog Mentions1
- Blog1
- References1
- Wikipedia1
Article Description
The striatum is widely viewed as the fulcrum of pathophysiology in Parkinsonâ €™ s disease (PD) and L-DOPA-induced dyskinesia (LID). In these disease states, the balance in activity of striatal direct pathway spiny projection neurons (dSPNs) and indirect pathway spiny projection neurons (iSPNs) is disrupted, leading to aberrant action selection. However, it is unclear whether countervailing mechanisms are engaged in these states. Here we report that iSPN intrinsic excitability and excitatory corticostriatal synaptic connectivity were lower in PD models than normal; L-DOPA treatment restored these properties. Conversely, dSPN intrinsic excitability was elevated in tissue from PD models and suppressed in LID models. Although the synaptic connectivity of dSPNs did not change in PD models, it fell with L-DOPA treatment. In neither case, however, was the strength of corticostriatal connections globally scaled. Thus, SPNs manifested homeostatic adaptations in intrinsic excitability and in the number but not strength of excitatory corticostriatal synapses.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84920795588&origin=inward; http://dx.doi.org/10.1038/ncomms6316; http://www.ncbi.nlm.nih.gov/pubmed/25360704; https://www.nature.com/articles/ncomms6316; https://dx.doi.org/10.1038/ncomms6316; http://www.nature.com/doifinder/10.1038/ncomms6316; http://www.nature.com/articles/ncomms6316.pdf; http://www.nature.com/articles/ncomms6316
Springer Science and Business Media LLC
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